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PubMed2001

[A case with trigeminal herpes zoster manifesting a long lesion of the spinal trigeminal nucleus and tract on MR T2-weighted image].

We reported a 53-year-old man with the right trigeminal herpes zoster with preceding neuralgia (preherpetic neuralgia) in the right upper cervical nerve area. He developed dysesthesia and scapular pain in the right second cervical nerve area. 5 days later, herpes zoster emerged in the area of the right maxillary division of trigeminal nerve. Furthermore, he developed paralysis on the right facial muscle on the 12th day after the onset of scapular pain. Neurological examination revealed decrease in superficial sensation accompanied by pain and dysesthesia in the areas innervated by the right maxillary division of trigeminal nerve and the right second cervical nerve, and the right peripheral facial nerve palsy. Any rash was not observed in the right second cervical nerve area throughout the course. The cerebrospinal fluid showed a mild mononuclear pleocytosis. The antibody titer for varicella zoster virus (VZV) was elevated in both cerebrospinal fluid and blood serum. T2-weighted magnetic resonance (MR) image revealed a continuously long high-signal lesion corresponding to the right spinal trigeminal nucleus and tract, extending from the lower pons to the second cervical segment of the spinal cord. This lesion could have resulted from a centripetal migration of VZV from the Gasser ganglion to the spinal trigeminal nucleus and tract, which was probably related to the preherpetic neuralgia in the upper cervical nerve area without rash.

Antibodies, Viral↗

PubMed1988

The chemotactic peptide receptor. A model for future understanding of chemotactic disorders.

Chemotaxis by human phagocytes enables these cells to find sites of injury or inflammation in the host. This function is a complex orchestration of biochemical and morphologic events that begins with the occupancy of specific surface receptors for chemotactic agents. The response is propagated and amplified by a biochemical cascade of transduction reactions. This cascade is mediated by receptor interactions with guanyl nucleotide binding proteins, subsequent activation of phospholipase C, and a resulting increase in phospholipid turnover. These events are spatially and temporarily integrated as elevations in the concentrations of intracellular Ca++ and diacylglycerol combine to activate protein kinase C. At the macromolecular and subcellular level, integration of these functions with as yet undiscovered pathways results in stimulation of actin polymerization, shape change, degranulation, and membrane flow. Final integration of these events results in the morphologic process of directed migration of the cell along concentration gradients of chemotaxins. During this process, chemotactic receptors are continuously regulated and feed back information to the response system that adjusts the biochemistry and morphology accordingly. This article has briefly considered some of the relationships between these transduction events and the control of a specific chemotactic receptor system employing the N-formylated chemotactic peptides. It is hoped that knowledge of this regulation will aid the physician in understanding the origin of chemotactic disorders derived from defects in chemotactic receptor systems of the phagocytic cells.

Calcium↗

PubMed2001

Mechanisms involved in the inhibition of neointimal hyperplasia by abciximab in a rat model of balloon angioplasty.

Monoclonal antibodies raised against beta(3) integrin are able to inhibit the binding of ligands to certain beta(3) integrins such as alpha(IIb)beta(3) (glycoprotein IIb/IIIa complex) and alpha(v)beta(3) (vitronectin receptor) and as such are inhibitors of platelet aggregation and smooth muscle cell (SMC) migration, both of which are involved in neointimal hyperplasia. The present study was designed to explore the detailed mechanisms of abciximab (Reopro), a monoclonal antibody (mAb) raised against alpha(IIb)beta(3) integrin in neointimal hyperplasia. In this study, carotid arteries of Wistar rats were damaged, and neointimal hyperplasia and lumen occlusion was determined at different time points. Abciximab was administered intravenously by an implanted osmotic pump. Abciximab (0.25 mg/kg/day) time-dependently inhibited both neointimal hyperplasia and lumen occlusion after angioplasty in carotid arteries of rats. Furthermore, the electromicrographs highlighted that SMCs were phenotypically different from the typical contractile, spindle-shaped SMCs normally seen in uninjured vessel walls. Platelet-derived growth factor (PDGF)-BB was strongly produced in thrombus formation and neointimal SMCs after angioplasty, while abciximab significantly reduced PDGF-BB expression in vessel lumens and neointimal SMCs after angioplasty. Balloon angioplasty caused a significant increase of nitrate and cyclic GMP as compared with sham-operated rats. Infusion of abciximab (0.25 mg/kg/day) did not significantly change. Furthermore, the plasma level of thromboxane B(2) (TxB(2)) obviously increased after angioplasty, while abciximab markedly suppressed the elevation of plasma TxB(2) concentration. The results indicate that abciximab effectively prevents neointimal hyperplasia, possibly through the following 2 mechanisms: (1) Abciximab binds to alpha(IIb)beta(3) integrin on platelet membranes resulting in inhibition of platelet adhesion, secretion, and aggregation in injured arteries, followed by inhibition of thromboxane A(2) formation and PDGF-BB release from platelets. (2) Abciximab may also bind to alpha(v)beta(3) integrin on SMCs, thus, subsequently inhibiting cell migration and proliferation.

Abciximab↗

PubMed2005

Macrophage migration inhibitory factor contributes to the development of acute dextran sulphate sodium-induced colitis in Toll-like receptor 4 knockout mice.

Toll-like receptor 4 (TLR4), which recognizes lipopolysaccharides, plays an important role in the innate immune response. In this study, we investigated the role of TLR4 in the development of experimental colitis with regard to the biological actions of macrophage migration inhibitory factor (MIF) using TLR4 null ((-/-)) mice. TLR4(-/-) mice were given 2% dextran sulphate sodium (DSS) in drinking water to induce colitis, which was clinically and histologically as severe as that seen in wild-type (WT) mice. The level of tumour necrosis factor (TNF)-alpha in colon tissues was increased in WT mice but unchanged in TLR4(-/-) mice. The level of myeloperoxidase (MPO) activity in colon tissues was increased by DSS administration in both TLR4(-/-) and WT mice. The expression of MIF was up-regulated in the colons of TLR4(-/-) mice with acute DSS-induced colitis. An anti-MIF antibody significantly suppressed colitis and elevation of matrix metalloproteinase-13 in TLR4(-/-) mice. The current results obtained from TLR4(-/-) mice provide evidence that MIF plays a critical role in the development of acute DSS-induced colitis.

Acute Disease↗

PubMed2004

Hypothyroidism caused by a nonvisible lingual thyroid.

BACKGROUND: Lingual thyroid is a developmental anomaly caused by failure of migration of the thyroid gland to its normal position in the neck. This anomaly is usually manifested in childhood as hypothyroidism or local symptoms. METHODS: We present a case of a 32-year-old patient in whom lingual thyroid was diagnosed after complaints of a chronic cough. Thyroid-stimulating hormone levels were significantly elevated. Sonograms of the neck revealed atrophy of both thyroid lobes, with nonhomogeneous consistency and no lymphadenopathy. Technetium-99m scan revealed uptake at the tongue base, with no uptake at the neck or other locations. RESULTS: L-thyroxine treatment was begun, with progressive decrement in thyroid-stimulating hormone levels and cessation of the cough. CONCLUSION: This case is unique in both the advanced age of the patient and the unusual clinical presentation.

Adult↗

PubMed2004

An uncomfortable silence em leader while we all search for a better reporter gene in adult stem cell biology.

The plasticity of bone marrow cells (BMCs) remains controversial. The present study found that persistent injury induces efficient trans-differentiation of BMCs into functional hepatocytes. Mice with liver cirrhosis induced by carbon tetrachloride were injected with 1 x 10(5) non-treated green fluorescent protein (GFP)-positive BMCs via the tail vein. In these mice, transplanted GFP-positive BMCs efficiently migrated into the peri-portal area of liver lobules after one day, repopulating 25% of the recipient liver by 4 weeks. In contrast, no GFP-positive BMCs were detected following transplantation into control mice with undamaged livers. BMCs trans-differentiated into functional mature hepatocytes via immature hepatoblasts. Serum albumin levels were significantly elevated to compensate for chronic liver failure in BMC transplantation. These results reveal that recipient conditions and microenvironments represent key factors for successful cell therapy using BMCs.

Comment↗

PubMed2005

Increased plasma MMP9 in integrin alpha1-null mice enhances lung metastasis of colon carcinoma cells.

Inhibitors of matrix metalloproteinases (MMPs) were developed as anticancer agents based on the observation that MMPs facilitate local tumor spread and metastasis by promoting matrix degradation and cell migration. Unfortunately, these inhibitors were unsuccessful in the clinical treatment of several cancers, including lung cancer. A possible reason contributing to their failure is that MMP activity is critical for the generation of inhibitors of tumor angiogenesis, including angiostatin. Thus, MMPs might play opposing roles in tumor vascularization and invasion. To determine which effect of elevated MMP levels dominates in the progression of metastatic cancer, experimental lung metastasis assays were performed in integrin alpha1-null mice, a genetic model for increased plasma levels of MMP9 and MMP9-generated angiostatin (Pozzi et al., Proc. Natl. Acad. Sci. USA 2000;97:2202-7). We show that while the number of lung colonies in integrin alpha1-null mice was significantly increased compared to their wild-type counterparts, tumor volume was markedly reduced. In vivo treatment with the MMP inhibitor doxycycline resulted in a significant decrease in the number of lung colonies in both genotypes, but the tumors that formed were bigger and more vascularized. Increased tumor vascularization paralleled decreased plasma levels of MMP9 and consequent decreased angiostatin synthesis. These results demonstrate that while inhibition of MMPs prevents and/or reduces tumor invasion and lung metastasis, it has the paradoxical effect of increasing the size and vascularization of metastatic tumors due to decreased generation of inhibitors of endothelial cell proliferation. The continued growth of these large well-vascularized tumors may explain the poor efficacy of MMP inhibitors in lung cancer clinical trials.

Angiogenesis Inhibitors↗

PubMed1996

Characterization of a new in vitro model for studies of reepithelialization in human partial thickness wounds.

Reepithelialization of artificial partial thickness wounds made in biopsies of human skin was determined after 3, 5, or 7 d of incubation, submerged or elevated to the air-liquid interface. The biopsies were reepithelialized within 5-7 d, with a more complete epidermal healing in wounds exposed to air. Both types of wounds showed similar time-course in deposition of basement membrane components, as detected by immunofluorescence labeling. Laminin and collagen type VII were deposited underneath the migrating tips, whereas collagen type IV was detected after reepithelialization. Markers of terminal differentiation showed a pattern close to normal in the air-liquid incubated wounds after reepithelialization. Involucrin was detected in the suprabasal regions of the migrating epidermis and thereafter in the upper half of neo-epidermis in the air-liquid incubated wound. Filaggrin could not be detected in the submerged wounds at any time during healing, whereas wounds exposed to air showed a well-differentiated epidermis by Day 7. Tritiated thymidine-incorporation indicated proliferation of epidermal and dermal cells during reepithelialization and a maintained viability, as shown by cultivation of endothelial- and fibroblast-like cells obtained from the dermis 7 d after wounding. Reepithelialization in this human in vitro model is supported by a matrix close to normal with the possibility of extracellular influences and cell-cell interactions and, in addition, the technique is simple and reproducible. Therefore, we suggest this model for studies of regeneration in culture and as a complement to in vivo studies on epidermal healing.

Basement Membrane↗

PubMed1999

Socio-demographic and spatial aspects of male mortality from HIV-AIDS related diseases in New South Wales, Australia, 1990-1994.

During 1990-1994, a very high proportion of males aged under 40 who died from HIV-AIDs related diseases in New South Wales were never married. However, a significant minority of men aged 40-64 who died had been married at some stage in their lives and in the cities of Newcastle, Wollongong and in higher income areas of Sydney this proportion approached 40%. AIDS related mortality was over-represented in professional, managerial, paraprofessional and service occupations even though educational levels were higher in these groups and, thus, presumably knowledge about risk behaviour and preventative behaviour. AIDS related mortality was also elevated among men with no stated occupation. Thus, with males, AIDS was in part a disease of affluence, even though the highest proportions of those dying resided in lower income areas, where marginalised persons may also be at risk. The proportion of deaths to men over age 40 was markedly higher than that in Australia in the 1980s. Elevated mortality with the New Zealand and the Americas birthplace groups may reflect overseas travel and exposure to risk in overseas countries, of persons domiciled in Australia. There was a very strong spatial pattern of AIDS-related mortality in the inner and eastern suburbs in Sydney and there is limited evidence of persons having migrated back to places of origin to be cared for by families. The impact on total mortality under age 65 in these localised areas was considerable. Prevention strategies should include the sensitive targeting of bisexual men, men generally having sex with men and those who are both gay and members of the drug sub-culture.

Adult↗

PubMed2001

Chronic systemic administration of salmeterol to rats promotes pulmonary beta(2)-adrenoceptor desensitization and down-regulation of G(s alpha).

1. The aim of the present study was to examine the effects of chronic infusion of the long-acting agonist salmeterol on pulmonary beta(2)-adrenoceptor function in Sprague-Dawley rats in vivo and to elucidate the molecular basis of any altered state. 2. Systemic administration of rats with salmeterol for 7 days compromised the ability of salmeterol and prostaglandin E(2) (PGE(2)), given acutely by the intravenous route, to protect against ACh-induced bronchoconstriction when compared to rats treated identically with vehicle. 3. beta(1)- and beta(2)-adrenoceptor density was significantly reduced in lung membranes harvested from salmeterol-treated animals, which was associated with impaired salmeterol- and PGE(2)-induced cyclic AMP accumulation ex vivo. 4. Three variants of G(s alpha) that migrated as 42, 44 and 52 kDa peptides on SDS polyacrylamide gels were detected in lung membranes prepared from both groups of rats but the intensity of each isoform was markedly reduced in rats that received salmeterol. 5. The activity of cytosolic, but not membrane-associated, G-protein receptor-coupled kinase was elevated in the lung of salmeterol-treated rats when compared to vehicle-treated animals. 6. The ability of salmeterol, administered systemically, to protect the airways of untreated rats against ACh-induced bronchoconstriction was short-acting (t(off) approximately 45 min), which contrasts with its long-acting nature when given to asthmatic subjects by inhalation. 7. These results indicate that chronic treatment of rats with salmeterol results in heterologous desensitization of pulmonary G(s)-coupled receptors. In light of previous data obtained in rats treated chronically with salbutamol, we propose that a primary mechanism responsible for this effect is a reduction in membrane-associated G(s alpha). The short-acting nature of salmeterol, when administered systemically, and the reduction in beta-adrenoceptor number may be due to metabolism to a biologically-active, short-acting and non-selective beta-adrenoceptor agonist.

Acetylcholine↗

PubMed2001

Rapid shoreward encroachment of salt marsh cordgrass in response to accelerated sea-level rise.

The distribution of New England salt marsh communities is intrinsically linked to the magnitude, frequency, and duration of tidal inundation. Cordgrass (Spartina alterniflora) exclusively inhabits the frequently flooded lower elevations, whereas a mosaic of marsh hay (Spartina patens), spike grass (Distichlis spicata), and black rush (Juncus gerardi) typically dominate higher elevations. Monitoring plant zonal boundaries in two New England salt marshes revealed that low-marsh cordgrass rapidly moved landward at the expense of higher-marsh species between 1995 and 1998. Plant macrofossils from sediment cores across modern plant community boundaries provided a 2,500-year record of marsh community composition and documented the migration of cordgrass into the high marsh. Isotopic dating revealed that the initiation of cordgrass migration occurred in the late 19th century and continued through the 20th century. The timing of the initiation of cordgrass migration is coincident with an acceleration in the rate of sea-level rise recorded by the New York tide gauge. These results suggest that increased flooding associated with accelerating rates of sea-level rise has stressed high-marsh communities and promoted landward migration of cordgrass. If current rates of sea-level rise continue or increase slightly over the next century, New England salt marshes will be dominated by cordgrass. If climate warming causes sea-level rise rates to increase significantly over the next century, these cordgrass-dominated marshes will likely drown, resulting in extensive losses of coastal wetlands.

Climate↗

PubMed1998

Control of exposure to airborne viable microorganisms during remediation of moldy buildings; report of three case studies.

Three different techniques for reducing exposure to microorganisms were tested during remediation of moldy buildings. Concentrations of spores (fungi and actinomycetes) were determined by filter sampling before, during, and after remediation. The local exhaust method used for asbestos dismantling was the most effective control method. In the construction zone, concentrations of microorganisms were 4-25 times higher during remediation than before it. In the adjacent area no increase in concentrations was seen. When the construction zone was placed under negative pressure with a fan and isolated with a plastic barrier, concentrations of microorganisms were about 100 times higher there during remediation work. Nevertheless, levels remained low in the adjacent area. The use of a portable exhaust fan with a side-draft hood decreased concentrations of fungi to one-tenth compared with demolition without the control technology. Furthermore, this method prevented the migration of fungal spores from the construction zone to the adjacent area, although it was less effective in prevention of actinomycete spore migration. It also decreased the levels of microorganisms in the construction zone below the preconstruction level within 2 hours. This study showed that levels of airborne microorganisms, including from the working area to adjacent area, can be reduced with commonly used dust control methods during demolition work. However, microorganism levels in the construction zone remained elevated. Therefore, personal protection of construction workers is needed even with control techniques.

Air Microbiology↗

PubMed2004

Down-regulation of plasminogen activator inhibitor 1 expression promotes myocardial neovascularization by bone marrow progenitors.

Human adult bone marrow-derived endothelial progenitors, or angioblasts, induce neovascularization of infarcted myocardium via mechanisms involving both cell surface urokinase-type plasminogen activator, and interactions between beta integrins and tissue vitronectin. Because each of these processes is regulated by plasminogen activator inhibitor (PAI)-1, we selectively down-regulated PAI-1 mRNA in the adult heart to examine the effects on postinfarct neovascularization and myocardial function. Sequence-specific catalytic DNA enzymes inhibited rat PAI-1 mRNA and protein expression in peri-infarct endothelium within 48 h of administration, and maintained down-regulation for at least 2 wk. PAI-1 inhibition enhanced vitronectin-dependent transendothelial migration of human bone marrow-derived CD34+ cells, and resulted in a striking augmentation of angioblast-dependent neovascularization. Development of large, thin-walled vessels at the peri-infarct region was accompanied by induction of proliferation and regeneration of endogenous cardiomyocytes and functional cardiac recovery. These results identify a causal relationship between elevated PAI-1 levels and poor outcome in patients with myocardial infarction through mechanisms that directly inhibit bone marrow-dependent neovascularization. Strategies that reduce myocardial PAI-1 expression appear capable of enhancing cardiac neovascularization, regeneration, and functional recovery after ischemic insult.

Adult↗

PubMed2003

An in vivo model for monitoring trans-differentiation of bone marrow cells into functional hepatocytes.

Albumins↗

PubMed2003

Restoring palpebral fissure shape after previous lower blepharoplasty.

The youthful palpebral fissure can be described as long and narrow. Both the aging process and transcutaneous lower blepharoplasty can cause descent of the lower lid margin and medial migration of the lateral canthus, resulting in a rounding of the palpebral fissure. This article presents a technique to correct significant postsurgical lower lid malposition and palpebral fissure distortion without the use of outer or inner lamellar grafts. In overview, subperiosteal dissection frees scarred lid structures and cheek soft tissues, creating a continuous composite flap. Elevation of the cheek soft tissues recruits deficient outer lamellae and allows the sub-orbicularis oculi fat to be positioned between the orbital rim and scarred lid structures, filling this space and helping to support the repositioned lid margin. Titanium screws placed in the lateral orbit provide a point for secure fixation of elevated cheek tissues. Transosseous wire fixation securely repositions the lateral canthus. This procedure not only restores lower lid position and the vertical height of the palpebral fissure, but it also restores the palpebral fissure's horizontal length and the lateral canthal angle. It has been effective in correcting palpebral fissure distortion after lower blepharoplasty in 15 patients during a 6-year period.

Adult↗

PubMed2002

Estimate of the subepithelial hydrostatic pressure that drives inflammatory transudate into the airway lumen.

Inflammatory diseases of the upper respiratory tract are characterized by flow of plasma filtrate across the epithelium into the airway lumen ("transudation"). Elsewhere, we have proposed that extravasation from microvessels causes edema, and this is associated with elevated subepithelial hydrostatic pressure that drives transudation. To test this hypothesis, we have attempted to block transudation by elevating luminal hydrostatic pressure. We measured the appearance of plasma markers into the lumen of an isolated perfused segment of rat trachea in vivo and found that stimulation of one vagal nerve caused a rapid (half-time approximately 5 min) and nonselective increase in the flow of markers from blood to airway lumen. Leukocyte migration also caused transudation that developed much more slowly (half-time = 2-3 h). In both cases, transudation was blocked by application of luminal hydrostatic pressures. The critical luminal pressure needed to block vagally induced transudation was approximately 4.5 cmH2O, and, to block epithelial transudation induced by leukocyte traffic, it was 3 cmH2O, and we conclude that these are the subepithelial pressures that drive inflammatory transudation into the airway lumen.

Albumins↗

PubMed2006

[Use of remote sensing to study the influence of environmental changes on malaria distribution in the Brazilian Amazon].

Construction of the Tucuruí hydroelectric dam in Southeast Pará State, Brazil, in 1981, caused enormous environmental changes, deforestation, and human migration to the region. This study focuses on the influence of these changes and the appearance of malaria in the municipality of Jacundá, Pará, using remote sensing and geographic information systems. The variables used to construct maps were distances from roads, farming areas, rivers, the dam, streams, and the urban area. This study confirmed the elevation of malaria to the epidemic level since the construction of the Tucuruí dam. The study suggests that a seasonal pattern of malaria incidence is associated with the flooding season and exposure of workers during harvest. Malaria cases were related to the form of land occupation, especially in more densely populated areas.

Biodegradation, Environmental↗

PubMed2004

Cutting edge: serotonin is a chemotactic factor for eosinophils and functions additively with eotaxin.

Elevated levels of serotonin (5-hydroxytryptamine, 5-HT) are observed in the serum of asthmatics. Herein, we demonstrate that 5-HT functions independently as an eosinophil chemoattractant that acts additively with eotaxin. 5-HT2A receptor antagonists (including MDL-100907 and cyproheptadine (CYP)) were found to inhibit 5-HT-induced, but not eotaxin-induced migration. Intravital microscopy studies revealed that eosinophils roll in response to 5-HT in venules under conditions of physiological shear stress, which could be blocked by pretreating eosinophils with CYP. OVA-induced pulmonary eosinophilia in wild-type mice was significantly inhibited using CYP alone and maximally in combination with a CCR3 receptor antagonist. Interestingly, OVA-induced pulmonary eosinophilia in eotaxin-knockout (Eot-/-) mice was inhibited by treatment with the 5-HT2A but not CCR3 receptor antagonist. These results suggest that 5-HT is a potent eosinophil-active chemoattractant that can function additively with eotaxin and a dual CCR3/5-HT2A receptor antagonist may be more effective in blocking allergen-induced eosinophil recruitment.

Adjuvants, Immunologic↗

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